Center for Musculoskeletal Research, University of Rochester School of Medicine and Dentistry, Rochester, USA.
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, USA.
Curr Osteoporos Rep. 2023 Oct;21(5):540-551. doi: 10.1007/s11914-023-00816-4. Epub 2023 Aug 5.
The purpose of this review is to summarize the recently published scientific literature regarding the effects of mitochondrial function and mitochondrial genome mutations on bone phenotype and aging.
While aging and sex steroid levels have traditionally been considered the most important risk factors for development of osteoporosis, mitochondrial function and genetics are being increasingly recognized as important determinants of bone health. Recent studies indicate that mitochondrial genome variants found in different human populations determine the risk of complex degenerative diseases. We propose that osteoporosis should be among such diseases. Studies have shown the deleterious effects of mitochondrial DNA mutations and mitochondrial dysfunction on bone homeostasis. Mediators of such effects include oxidative stress, mitochondrial permeability transition, and dysregulation of autophagy. Mitochondrial health plays an important role in bone homeostasis and aging, and understanding underlying mechanisms is critical in leveraging this relationship clinically for therapeutic benefit.
本文综述了近期发表的关于线粒体功能和线粒体基因组突变对骨骼表型和衰老影响的科学文献。
虽然衰老和性激素水平一直被认为是骨质疏松症发展的最重要危险因素,但线粒体功能和遗传学正越来越被认为是骨骼健康的重要决定因素。最近的研究表明,不同人群中发现的线粒体基因组变异决定了复杂退行性疾病的风险。我们提出骨质疏松症也应属于此类疾病。研究表明,线粒体 DNA 突变和线粒体功能障碍对骨稳态有有害影响。这些影响的介导因素包括氧化应激、线粒体通透性转换和自噬失调。线粒体健康在骨骼稳态和衰老中起着重要作用,理解其潜在机制对于从临床角度利用这种关系获得治疗益处至关重要。